Key result
Continuous infusion of digoxin in anaesthetized dogs increased myocardial contractility by up to 30% above control levels at a cumulative dose of 35 μg/kg.
Why the study?
Does continuous infusion of digoxin increase myocardial contractility in anaesthetized dogs with nonfailing hearts?
Does continuous infusion of digoxin increase myocardial contractility in anaesthetized dogs with nonfailing hearts?
Answers are grounded in this paper and cite their sources.
In a canine model, maximal increase in myocardial contractility is achieved at a myocardial digoxin content of approximately 140 ng/g tissue, with no dysrhythmias observed at levels up to 275 ng/g.
The effect of digoxin on the contractility of the nonfailing heart was studied in anaesthetized dogs receiving continuous infusion of digoxin 0.8 jig/kg/ min. The contractility, described by V ce5 was increased to 30 % above control levels after infusion of 35 μg/kg of digoxin. From this point only an insignificant increase in contractility was obtained following futher infusion of digoxin. The myocardial content of digoxin, measured by a radio immuno method, was proportional to the cummulated dose and calculated to be about 140 ng/g tissue, when the maximal increase in contractility was achieved. The content of digoxin in the myocardium of 275 ng/g tissue was not associated with dysrhythmias.
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Videbæk et al. (1974) studied nonfailing heart. Digoxin vs. control levels was evaluated on contractility (V ce5). Continuous infusion of digoxin in anaesthetized dogs increased myocardial contractility by up to 30% above control levels at a cumulative dose of 35 μg/kg.
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